Morphine modulates proliferation of kidney fibroblasts

Singhal, Pravin C.; Sharma, Pratima; Sanwal, Vibha; Prasad, Abhinav; Kapasi, Aditi A.; Ranjan, Rajiv; Franki, Nicholas; Reddy, Krishna; Gibbons, Nora

doi:10.1046/j.1523-1755.1998.00758.x

Cited by 86 publications

(60 citation statements)

References 25 publications

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“…While the rest are changed into active metabolites by the liver. Metabolites of the drug that are excreted via kidneys may also cause cellular damage leading to kidney dysfunction [24].…”

Section: Discussionmentioning

confidence: 99%

Histopathological and Biochemical Effects of Acute & Chronic Tramadol drug Toxicity on Liver, Kidney and Testicular Function in Adult Male Albino Rats

2016

FRCIJ

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Background: Tramadol is becoming abused among teens; especially between males. The study aimed to investigate the histopathological and biochemical profiles of acute and chronic toxic effects of tramadol on hepatic, renal and testicular functions.Methodology: Sixty male adult albino Sprague-Dawley rats were used. Rats were divided into three groups. Group I: control. Group II: representing acute tramadol toxicity and group III: representing tramadol dependent use for 60 days.Results: Group II displayed hemorrhage and cytolysis in the hepatocytes. Group III showed complete cell membrane degeneration of hepatocytes. Renal tissues revealed glomerular hemorrhage in group II and atrophied glomerulus with collapsed tufts, degenerated tubules and cellular infiltration in group III. The testicular tissues revealed atrophy of seminiferous tubules with interstitial calcification in group II. Focal testicular degeneration, with a little evidence of spermatogenesis in group III. Biochemical indices showed significant increase in liver enzymes, serum bilirubin, creatinine and blood urea nitrogen levels. The sex hormones levels were significantly increased for estradiol and prolactin, while there was a significant decrease in testosterone with a gradual reduction in luteinizing and follicular stimulating hormones.Recommendations: Designing a national awareness campaign to the youth to spotlights on the health hazards of tramadol abuse.

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“…While the rest are changed into active metabolites by the liver. Metabolites of the drug that are excreted via kidneys may also cause cellular damage leading to kidney dysfunction [24].…”

Section: Discussionmentioning

confidence: 99%

Histopathological and Biochemical Effects of Acute & Chronic Tramadol drug Toxicity on Liver, Kidney and Testicular Function in Adult Male Albino Rats

2016

FRCIJ

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“…At lower concentrations, morphine predominantly stimulates mesangial cell and fibroblast proliferation, mesangial matrix deposition, and macrophage activity. At higher concentrations, morphine inhibits mesangial cell and fibroblast proliferation, mesangial matrix deposition, and macrophage activity (185)(186)(187)(188)(189).…”

Section: Direct Effects Of Heroin/morphine On the Kidney: Pathophysiomentioning

confidence: 99%

Chronic Nephropathies of Cocaine and Heroin Abuse

Jaffe

Kimmel²

2006

Clinical Journal of the American Society of Nephrology

124

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Renal disease in cocaine and heroin users is associated with the nephrotic syndrome, acute glomerulonephritis, amyloidosis, interstitial nephritis, and rhabdomyolysis. The pathophysiologic basis of cocaine-related renal injury involves renal hemodynamic changes, glomerular matrix synthesis and degradation, and oxidative stress and induction of renal atherogenesis. Heroin is the most commonly abused opiate in the United States. Previous studies identified a spectrum of renal diseases in heroin users. The predominant renal lesion in black heroin users is focal segmental glomerulosclerosis and in white heroin users is membranoproliferative glomerulonephritis. Although the prevalence of heroin use in the United States has increased, the incidence of "heroin nephropathy" has declined. Because reports of heroin nephropathy predated the surveillance of hepatitis C virus and HIV, the varied findings might be related to the spectrum of viral illnesses that are encountered in injection drug users. Socioeconomic conditions, cultural and behavioral practices, or differences in genetic susceptibilities may be more associated with the development of nephropathy in heroin users than the drug's pharmacologic properties. Administration of cocaine in animal models results in nonspecific glomerular, interstitial, and tubular cell lesions, but there is no animal model of heroin-associated renal disease. The heterogeneity of responses that are associated with heroin is not consistent with a single or simple notion of nephropathogenesis. There are no well-designed, prospective, epidemiologic studies to assess the incidence and the prevalence of renal disease in populations of opiate users and to establish the validity of a syndrome such as heroin nephropathy. It is concluded although there is a paucity of evidence to support a heroinassociated nephropathy, the evidence from in vitro cellular and animal studies to support the existence of cocaine-induced renal changes is more convincing.

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“…They suggested that this effect was mediated through a neurotrophic mechanism or inhibition of neurotransmission (Meriney et al, 1985). Morphine also prevented peroxynitrite-induced apoptosis in primary astrocytes (Kim et al, 2001) and enhanced the proliferation of endothelial cells (Gupta et al, 2002), kidney fibroblasts (Singhal et al, 1998), and adult hippocampal progenitor neurons (Persson et al, 2003). In addition, dynorphin (KOR agonist) and DOR agonists were found to increase proliferation of prostate cancer cells (Moon, 1988), rat splenocytes (Ni et al, 1999), and neuroblastoma cells (Law and Bergsbaken, 1995;Law et al, 1997), respectively.…”

Section: Growth-promoting and Protective Effectsmentioning

confidence: 99%